scholarly journals Peripheral sensitization and neuropathic pain in the rat medial meniscal tear model of post-traumatic osteoarthritis

2018 ◽  
Vol 26 ◽  
pp. S357
Author(s):  
M.S. O'Brien ◽  
C. DeBow ◽  
J.J. McDougall
Keyword(s):  
Neuropathic Pain ◽  
Meniscal Tear ◽  
Peripheral Sensitization ◽  
Medial Meniscal Tear ◽  
Post Traumatic

scholarly journals Topical Treatments and Their Molecular/Cellular Mechanisms in Patients with Peripheral Neuropathic Pain—Narrative Review

Pharmaceutics ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 450
Author(s):  
Magdalena Kocot-Kępska ◽  
Renata Zajączkowska ◽  
Joanna Mika ◽  
David J. Kopsky ◽  
Jerzy Wordliczek ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Pain Management ◽  
Clinical Studies ◽  
Neuronal Cells ◽  
Case Series ◽  
Narrative Review ◽  
Peripheral Sensitization ◽  
Cellular Mechanisms ◽  
Peripheral Neuropathic Pain ◽  
Topical Treatments

Neuropathic pain in humans results from an injury or disease of the somatosensory nervous system at the peripheral or central level. Despite the considerable progress in pain management methods made to date, peripheral neuropathic pain significantly impacts patients’ quality of life, as pharmacological and non-pharmacological methods often fail or induce side effects. Topical treatments are gaining popularity in the management of peripheral neuropathic pain, due to excellent safety profiles and preferences. Moreover, topical treatments applied locally may target the underlying mechanisms of peripheral sensitization and pain. Recent studies showed that peripheral sensitization results from interactions between neuronal and non-neuronal cells, with numerous signaling molecules and molecular/cellular targets involved. This narrative review discusses the molecular/cellular mechanisms of drugs available in topical formulations utilized in clinical practice and their effectiveness in clinical studies in patients with peripheral neuropathic pain. We searched PubMed for papers published from 1 January 1995 to 30 November 2020. The key search phrases for identifying potentially relevant articles were “topical AND pain”, “topical AND neuropathic”, “topical AND treatment”, “topical AND mechanism”, “peripheral neuropathic”, and “mechanism”. The result of our search was 23 randomized controlled trials (RCT), 9 open-label studies, 16 retrospective studies, 20 case (series) reports, 8 systematic reviews, 66 narrative reviews, and 140 experimental studies. The data from preclinical studies revealed that active compounds of topical treatments exert multiple mechanisms of action, directly or indirectly modulating ion channels, receptors, proteins, and enzymes expressed by neuronal and non-neuronal cells, and thus contributing to antinociception. However, which mechanisms and the extent to which the mechanisms contribute to pain relief observed in humans remain unclear. The evidence from RCTs and reviews supports 5% lidocaine patches, 8% capsaicin patches, and botulinum toxin A injections as effective treatments in patients with peripheral neuropathic pain. In turn, single RCTs support evidence of doxepin, funapide, diclofenac, baclofen, clonidine, loperamide, and cannabidiol in neuropathic pain states. Topical administration of phenytoin, ambroxol, and prazosin is supported by observational clinical studies. For topical amitriptyline, menthol, and gabapentin, evidence comes from case reports and case series. For topical ketamine and baclofen, data supporting their effectiveness are provided by both single RCTs and case series. The discussed data from clinical studies and observations support the usefulness of topical treatments in neuropathic pain management. This review may help clinicians in making decisions regarding whether and which topical treatment may be a beneficial option, particularly in frail patients not tolerating systemic pharmacotherapy.

scholarly journals Arthroscopic Articular Cartilage Scores of the Canine Stifle Joint with Naturally Occurring Cranial Cruciate Ligament Disease

2020 ◽  
Author(s):  
Kimberly A. Agnello ◽  
Kei Hayashi ◽  
Dorothy Cimino Brown
Keyword(s):  
Articular Cartilage ◽  
Cruciate Ligament ◽  
Cartilage Damage ◽  
Meniscal Tear ◽  
Trochlear Groove ◽  
Cranial Cruciate Ligament ◽  
Stifle Joint ◽  
Naturally Occurring ◽  
Medial Meniscal Tear ◽  
Severity Scores

Abstract Objective This study aimed to evaluate frequency, location and severity of cartilage pathology in dogs with naturally occurring cranial cruciate ligament (CCL) disease. Study Design Stifle arthroscopic video recordings (n = 120) were reviewed. A modified Outerbridge classification system (MOCS) (0–4) was used to score cartilage at 10 locations in the femorotibial (medial and lateral femoral condyles and tibial plateaus) and patellofemoral compartments (proximal, middle and distal locations of the patella and femoral trochlear groove) of the stifle joint. Synovial pathology was scored and the presence of a medial meniscal tear was recorded. A Kruskal–Wallis test was used to evaluate association of location and synovitis with cartilage score; and presence of meniscal tear with cartilage and synovitis scores. Bonferroni correction was utilized and p < 0.05 was considered significant. Results Cartilage pathology and synovitis were identified in all joints. Overall cartilage severity scores were low (median MOCS 1). The median MOCS of the proximal trochlear groove (2) was significantly higher than all other locations evaluated. Higher synovitis scores were significantly associated with higher cartilage severity scores and a medial meniscal tear had no association with cartilage severity scores or synovitis. Conclusion Arthroscopic articular cartilage lesions are common in dogs with CCL disease at the time of surgical intervention, although the severity of cartilage damage is mild. The proximal trochlear groove of the femur had the most severe cartilage score in the stifle joint.

Medial Meniscal Tear

2010 ◽  
pp. 147
Author(s):  
Joel A. Vilensky ◽  
Edward C. Weber ◽  
Thomas E. Sarosi ◽  
Stephen W. Carmichael
Keyword(s):  
Meniscal Tear ◽  
Medial Meniscal Tear

scholarly journals Overexpression of P2X3 and P2X7 Receptors and TRPV1 Channels in Adrenomedullary Chromaffin Cells in a Rat Model of Neuropathic Pain

2019 ◽  
Vol 20 (1) ◽  
pp. 155 ◽  
Author(s):  
Marina Arribas-Blázquez ◽  
Luis Alcides Olivos-Oré ◽  
María Victoria Barahona ◽  
Mercedes Sánchez de la Muela ◽  
Virginia Solar ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Nicotinic Acetylcholine Receptors ◽  
Chromaffin Cells ◽  
Transient Receptor Potential ◽  
Synaptic Activity ◽  
Cholinergic Innervation ◽  
Cell Junction ◽  
Transient Receptor Potential Vanilloid ◽  
Peripheral Sensitization ◽  
Trpv1 Channels

We have tested the hypothesis that neuropathic pain acting as a stressor drives functional plasticity in the sympathoadrenal system. The relation between neuropathic pain and adrenal medulla function was studied with behavioral, immunohistochemical and electrophysiological techniques in rats subjected to chronic constriction injury of the sciatic nerve. In slices of the adrenal gland from neuropathic animals, we have evidenced increased cholinergic innervation and spontaneous synaptic activity at the splanchnic nerve–chromaffin cell junction. Likewise, adrenomedullary chromaffin cells displayed enlarged acetylcholine-evoked currents with greater sensitivity to α-conotoxin RgIA, a selective blocker of α9 subunit-containing nicotinic acetylcholine receptors, as well as increased exocytosis triggered by voltage-activated Ca2+ entry. Altogether, these adaptations are expected to facilitate catecholamine output into the bloodstream. Last, but most intriguing, functional and immunohistochemical data indicate that P2X3 and P2X7 purinergic receptors and transient receptor potential vanilloid-1 (TRPV1) channels are overexpressed in chromaffin cells from neuropathic animals. These latter observations are reminiscent of molecular changes characteristic of peripheral sensitization of nociceptors following the lesion of a peripheral nerve, and suggest that similar phenomena can occur in other tissues, potentially contributing to behavioral manifestations of neuropathic pain.

Pain neurophysiology

2013 ◽  
Author(s):  
Hans-Georg Schaible ◽  
Rainer H. Straub
Keyword(s):  
Neuropathic Pain ◽  
Central Sensitization ◽  
Cell Activation ◽  
Warning Signal ◽  
Nociceptive Pain ◽  
Neural Function ◽  
Peripheral Sensitization ◽  
Nerve Fibres ◽  
Glial Cell Activation ◽  
Ectopic Discharges

Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.

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